Stroke is the leading cause of long term disability in the United States and the second leading cause of death worldwide with over 4.4 million deaths in a year (1999).1 There are over 700,000 new strokes every year in the United States.2 Around 85% of all strokes are acute ischemic strokes caused from a blockage in a blood vessel or a blood clot occluding a blood vessel.2 In 1996, the FDA approved a thrombolytic drug to dissolve blood clots called recombinant tissue plasminogen activator (r-tpa).3 Despite practice guidelines from multiple national organizations stating the intravenous r-tpa is the standard of care for patients with acute ischemic stroke within 3 hours from symptom onset,3 only 3-4% of patients with acute ischemic stroke received this drug in the United States.4 Unlike intravenous r-tpa, Intra-arterial infusion of thrombolytic agents can be used for up to 6 hours from acute ischemic stroke symptom onset and could benefit more people.5 Currently, intra-arterial infusion of thrombolytic agents are administered to a blood clot and the blood clot breaks up into smaller blood clots and travel downstream and potentially close up smaller cerebral blood vessels. With advances in regional stroke networks, there are more and more stroke patients who are getting access to intra-arterial thrombolysis and therapies, and are as high as 21.6%.4 However, there is no currently available distal embolic protection device that is dedicated to the cerebral blood vessels.
More than 8% of all acute ischemic strokes are from blockages in the cervical or neck carotid artery.2 Studies have shown that performing percutaneous balloon angioplasty and stenting on these blockages result in emboli or debris being dislodged downstream and could cause further strokes and therefore there have been large clinical trials of angioplasty and stenting of the carotid artery in the neck with distal embolic protection devices being used.6 In addition to blockages in the neck region of the carotid artery, more than 8% of all acute ischemic strokes are due to blockages in the cerebral arterial blood vessels called intracranial stenosis.2 Recently there has been a new device approved for intracranial angioplasty and stenting.7 Although the risks of small emboli or debris being dislodged during intracranial angioplasty and stenting is similar to the cervical carotid artery and the rest of the body, there are no distal embolic protection devices in the market dedicated for cerebral arterial blood vessels. In addition, the distal embolic protection devices currently available for the cervical carotid artery are too bulky for use in the tortuous and fragile cerebral arterial blood vessels.
Embolic protection devices have been developed for the cervical carotid artery prior to carotid angioplasty and stenting.6 However, these devices do not have a small profile for use in the cerebral arterial blood vessels and will not be able to track and traverse the tortuous cerebral arterial blood vessels.
Barbut in U.S. Pat. No. 6,165,199 has described embolic protection devices that can be used for the cerebral arterial blood vessels. This is a proximal embolic protection device wherein the embolic protection device is before the clot or blockage comprising of a proximal balloon occlusion catheter to create flow arrest and an aspiration device to suction out the emboli or debris during the interventional procedure in the cervical and cerebral blood vessels. The drawbacks of a proximal protection device are that the flow arrest performed to decrease emboli or debris from traveling downstream can be detrimental in itself, since creating a flow arrest in an already ischemic blood vessel during the long neurovascular interventional procedures would in itself worsen the cerebral ischemia and worsen the strokes. Bose et al in U.S. Pat. No. 6,669,721 describe thin-film distal embolic protection devices that can be potentially used in the cerebral blood vessels. The device has one or two rings and a thin-film filter that is attached to the guidewire. The drawbacks of this device is that during neurovascular interventional procedures, there is constant exchange of microcatheters, balloon catheters, and stent catheters over the guidewire or microguidewire, and a distal embolic protection device that is rigidly fixed to the guidewire or microguidewire would cause trauma to the cerebral arterial blood vessel wall as there will not be any mobility of the wire independent of the distal embolic protection device. Hopkins et al in U.S. Pat. No. 6,544,279 B1 describe distal embolic protection devices that do have mobility over a guidewire or microguidewire, however these guidewires or microguidewires are of uniform thickness and the mobile attachment point in these devices extend through the entire length of the device. Current microguidewires used in neurovascular interventional procedures to perform intracranial angioplasty and stenting among other procedures use microguidewires in the thickness of 0.014 inch (0.356 mm).7 Current microcatheters used for intracranial cerebral blood vessel catheterization for stroke as well as during intracranial angioplasty and stenting have an inner diameter of about 0.017 inch (0.432 mm). Having a distal embolic protection device mounted on a uniform thickness microguidewire of a thickness of 0.014 inch (0.356 mm) will not permit the distal embolic protection device in the collapsed form to have a thin enough or small enough profile to be compatible with existing microcatheters that are 0.017 inch (0.432 mm) in inner diameter. Having a distal embolic protection device mounted on a uniform thickness microguidewire with a mobile attachment point that extends through the entire length of the device will increase the overall thickness of the device in the collapsed configuration thereby limiting the trackability of the device and inhibiting access to the tortuous and narrow cerebral arterial blood vessels.